Pneumocystis Pneumonia -- Los Angeles

In the period October 1980-May 1981, 5 young men, all active homosexuals,
were treated for biopsy-confirmed Pneumocystis carinii pneumonia at 3
different hospitals in Los Angeles, California. Two of the patients died. All 5
patients had laboratory-confirmed previous or current cytomegalovirus (CMV)
infection and candidal mucosal infection. Case reports of these patients follow.

Patient 1: A previously healthy 33-year-old man developed P. carinii
pneumonia and oral mucosal candidiasis in March 1981 after a 2-month history of
fever associated with elevated liver enzymes, leukopenia, and CMV viruria. The
serum complement-fixation CMV titer in October 1980 was 256; in may 1981 it was
32.* The patient's condition deteriorated despite courses of treatment with
trimethoprim-sulfamethoxazole (TMP/SMX), pentamidine, and acyclovir. He died May
3, and postmortem examination showed residual P. carinii and CMV
pneumonia, but no evidence of neoplasia.

Patient 2: A previously healthy 30-year-old man developed p. carinii
pneumonia in April 1981 after a 5-month history of fever each day and of
elevated liver-function tests, CMV viruria, and documented seroconversion to CMV,
i.e., an acute-phase titer of 16 and a convalescent-phase titer of 28* in
anticomplement immunofluorescence tests. Other features of his illness included
leukopenia and mucosal candidiasis. His pneumonia responded to a course of
intravenous TMP/.SMX, but, as of the latest reports, he continues to have a
fever each day.

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Patient 3: A 30-year-old man was well until January 1981 when he developed
esophageal and oral candidiasis that responded to Amphotericin B treatment. He
was hospitalized in February 1981 for P. carinii pneumonia that responded
to TMP/SMX. His esophageal candidiasis recurred after the pneumonia was
diagnosed, and he was again given Amphotericin B. The CMV complement-fixation
titer in March 1981 was 8. Material from an esophageal biopsy was positive for
CMV.

Patient 4: A 29-year-old man developed P. carinii pneumonia in
February 1981. He had had Hodgkins disease 3 years earlier, but had been
successfully treated with radiation therapy alone. He did not improve after
being given intravenous TMP/SMX and corticosteroids and died in March.
Postmortem examination showed no evidence of Hodgkins disease, but P. carinii
and CMV were found in lung tissue.

Patient 5: A previously healthy 36-year-old man with clinically diagnosed CMV
infection in September 1980 was seen in April 1981 because of a 4-month history
of fever, dyspnea, and cough. On admission he was found to have P. carinii
pneumonia, oral candidiasis, and CMV retinitis. A complement-fixation CMV titer
in April 1981 was 128. The patient has been treated with 2 short courses of TMP/SMX
that have been limited because of a sulfa-induced neutropenia. He is being
treated for candidiasis with topical nystatin.

The diagnosis of Pneumocystis pneumonia was confirmed for all 5
patients antemortem by closed or open lung biopsy. The patients did not know
each other and had no known common contacts or knowledge of sexual partners who
had had similar illnesses. Two of the 5 reported having frequent homosexual contacts
with various partners. All 5 reported using inhalant drugs, and 1 reported
parenteral drug abuse. Three patients had profoundly depressed in vitro
proliferative responses to mitogens and antigens. Lymphocyte studies were not
performed on the other 2 patients.

Editorial Note

Pneumocystis pneumonia in the United States is
almost exclusively limited to severely immunosuppressed patients.1 The
occurrence of pneumocystosis in these 5 previously healthy individuals without a
clinically apparent underlying immunodeficiency is unusual. The fact that these
patients were all homosexuals suggests an association between some aspect of a
homosexual lifestyle or disease acquired through sexual contact and Pneumocystis
pneumonia in this population. All 5 patients described in this report had
laboratory-confirmed CMV disease or virus shedding within 5 months of the
diagnosis of Pneumocystis pneumonia. CMV infection has been shown to
induce transient abnormalities of in vitro cellular-immune function in
otherwise healthy human hosts.2,3 Although all 3 patients tested had abnormal
cellular-immune function, no definitive conclusion regarding the role of CMV
infection in these 5 cases can be reached because of the lack of published data
on cellular-immune function in healthy homosexual males with and without CMV
antibody. In 1 report, 7 (3.6%) of 194 patients with pneumocystosis also had CMV
infection' 40 (21%) of the same group had at least 1 other major concurrent
infection.1 A high prevalence of CMV infections among homosexual males was
recently reported: 179 (94%) had CMV viruria; rates for 101 controls of similar
age who were reported to be exclusively heterosexual were 54% for seropositivity
and zero fro viruria.4 In another study of 64 males, 4 (6.3%) had positive
tests for CMV in semen, but none had CMV recovered from urine. Two of the 4
reported recent homosexual contacts. These findings suggest not only that virus
shedding may be more readily detected in seminal fluid than urine, but also that
seminal fluid may be an important vehicle of CMV transmission.5

All the above observations suggest the possibility of a cellular-immune
dysfunction related to a common exposure that predisposes individuals to
opportunistic infections such as pneumocystosis and candidiasis. Although the
role of CMV infection in the pathogenesis of pneumocystosis remains unknown, the
possibility of P. carinii infection must be carefully considered in a
differential diagnosis for previously healthy homosexual males with dyspnea and
pneumonia.

M.S. Gottlieb, M.D., H.M. Schanker, M.D., P.T. Fan, M.D., A. Saxon, M.D. and J.D. Weisman, D.O., are with the Division of Clinical Immunology-Allergy at the Department of Medicine, UCLA School of Medicine. I. Pozalski, M.D., is with the Cedars-Mt. Siani Hospital, Los Angeles and the Field
Services Division, Epidemiology Program Office at the CDC.

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